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2. CONTENTS:
1. INTRODUCTION
2. EPIDEMIOLOGY
3. ETIOLOGY
4. EMBRYOLOGY
5. CLASIFICATION OF CLEFTS
6. TREATMENT OF CLEFT LIP AND PALATE:
- INFANT ORTHOPEDICS
- TREATMENT IN MIXED DENTITION
- ALVEOLAR BONE GRAFTING
- TREATMENT IN PERMANENT DENTITION
- SURGICAL ORTHODONTICS
- DISTRACTION OSTEOGENESIS
7. CONCLUSION
8. REFERENCES
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3. INTRODUCTION
Cleft of lip and the palate is among the most common
congenital anomalies requiring multidisciplinary care.
Such anomalies include several handicaps such as
impaired suckling, defective speech, deafness,
malocclusion, gross facial deformity and severe
psychological problems.
Management of CLCP involves a multi disciplinary
approach requiring the services of an orthodontist,
oral surgeon, prosthodontist, audiologist, speech
therapist, paediatrician.
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4. EPIDEMIOLOGY:
Cleft lip and palate is a global problem ( 0.28-3.74/1000
live births globally ).
Least incidence in negroids(0.4%) and maximum in
afghans(4.9%)
Among Indians it seen maximum in Aggarwal community
and Brahmins(1.7%).
The incidence of oral clefts is seen more in males than in
females.
Cleft lip alone - more in males than female.
Cleft palate - more in females than males.
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5. INCIDENCE
Oral clefts occur with an incidence of 1 in 750 live births,
making clefts the second most common congenital defect.2
Family studies have shown that siblings of patients with Cleft
Lip or Palate have an increased incidence of same, but the same
is not true of isolated CP.
The siblings of patients with CP have an increased frequency of
CP but not of CL/P. There is a male excess in CL/ P and a
female excess in CP (Fogh Andersen, 1942). Those clefts
extending more anteriorly towards incisive foramen are
common in females.3
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6. In INDIA, the survey conducted by Christian Medical
College, Vellore reported the incidence of Cleft Lip and
Palate in the regional population as 1:639.
A ten year retrospective study (1980-90) at the ‘College of
Dental Surgery, Kasturba Medical College9
, Manipal,
Karnataka’ by Shetty and Valiathan, reported the incidence of
1:809 (1.23 per 1000) for CL/P, 1: 6065 (0.16 per 1000) for
Isolated Cleft Lip and 1:12145 (0.08 per 1000) for Isolated
Cleft Palate in regional population.
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7. The relative frequency of CL and CP in India is about 4:1.4
Unilateral Clefts are more common than bilateral clefts. In
Delhi, India; it is 2.21:1.4
Left side is more frequently involved as compared to right
side. 4
In India, the incidence of CL/ P was found to be 87.6% in
Hindus, 9.5% in Muslims and 3.8% in Christians.4
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8. RACIAL INFLUENCES
Although the Caucasian race has been the most
extensively studied, statistics are available for the
incidence of cleft lip and palate in the Black and
Oriental races.
Mean incidence of CL/P in Caucasians is
approximately 1 per 1000 populations (Fraser,
1970).
A higher frequency of CL/P among Japanese infants
was reported as approximately 2.1 per 1000; the
incidence rate for CP was 0.00055 (Neel, 1958) 3
.
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9. INCIDENCE OF CLEFT LIP AND / OR PALATE PER
THOUSAND LIVE BIRTHS9
INDIANS 1.7
CAUCASIANS 1
JAPANESE 1.7
NEGROIDS 0.4
AMERICAN INDIAN 3.6
AFGHANS 4.9
CZECHOSLOVAKIA
(ERSTWHILE)
1.85
DENMARK 1.1
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10. ETIOLOGY
Trew (1951)9
first recognized heredity as a pre-disposing
factor to CL/P.
Adams and Niswander (1976)9
first discussed the
environmental effects and developmental alterations .
Gortlin et al (1971)9
described approx.100 syndromes which
had CL/P.
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11. Associated Syndromes are:
Pierre Robin Syndrome.
Stickler.
Velo-cardio-facial.
Van der Woude.
Goldenhaar.
Treacher- Collins
Ectrodactyly- ectosdermal dysplasia- cleft.
Oro-facial- Digital.
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12. The causes3
of cleft lip and palate include –
Anterior neural plate development and positioning of olfactory
placodes.
Extirpation / killing of neural crest cells.
Genetic factors.
Environmental factors.
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13. 1. Anterior Neural Plate Development and positioning of
Olfactory (Nasal) Placodes3
.
Malformations in the Facial defect may include mild
midfacial underdevelopment, typical CL/P, and more
severe defects. The deficiencies may be due to
deformities of the midline region of the anterior neural
plate.
Cleft lip may develop due to failure of the maxillary
processes to meet the median frontal process.
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14. Failure may be due to delay in the timing when these
processes are to meet. One of the processes may have
developed too slowly. The processes may then fail to fuse.
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15. II. Extirpation or Killing of Neural Crest
Cells.3
If crest cells are denatured or malformed before or at the
beginning of their migration, there is reduction of the facial
mesenchyme and size of the facial prominences.
Thus, prominences do not contact to form the lips and
associated structures. However, this may not produce non-
syndromic human CL(P).
CL/P associated with Waardenburg's syndrome may be present
if only crest cell derivatives are involved.
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17. Genetic Factors 3
:
Certain genetic effects depend on the environment
mother provides for the embryo, thereby, predisposing
the embryo to CL/P.
Anatomical and physiological variations of the uterus,
the endocrine make-up (blood supply to the fetus,
pressure on the fetus) and characteristics like
metabolic alterations in mother body may lead to
development of CL/P in fetus.
Most hormones and metabolic products cross the
placenta and may influence development of embryo.
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18. Cigarette smoking during pregnancy in the first trimester is
also associated with increased risk of Cleft Lip/Palate.
A single major recessive gene is primarily responsible for the
genetic predisposition.
The abnormal placode positioning also contributes to
malformations.
Deficiencies of the medial nasal processes lead to various
defects, like Fetal Alcohol syndrome and Cleft lip.
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19. If both parents are not affected with cleft- there is 4% risk of
the child to develop Cleft Lip and 2% risk for Cleft Palate.6
If both parents are affected with cleft, then, 50-60% risk of
developing cleft. 6
If one child is affected with CL/P, then 15-20% risk for next
child to develop the CL/P. 6
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20. BOTH MOTHER AND CHILD AFFECTED WITH
CLEFT LIP & PALATE
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21. ENVIRONMENTAL
FACTORSThey include7
:
1. Viral infections.
2. Exposure to radiations.
3. Influence of Drugs: Phenytoin, Steroids, Anti-epileptics.
4. Deficiency of Vitamins A and B.
5. Anemia.
6. Anorexia.
7. Stress.
8. Excessive Consumption of Alcohol.
9. Excessive Tobacco Chewing.
10. Maternal Age: Older the mother, greater will be the chances
of incidence of congenital anomalies and hence, CL/P, since
there is a defective zygote.9
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22. HYPOXIA – INDUCED CL/P3
Environmental factors like hypoxia and carbon monoxide
(CO) inhibit the electron transport chain3
(and thus, ATP
production) which may lead to CL/P in mammals.
Hypoxia-induced CL/P has been extensively studied by
Bronsky, Johnston, and Sulik, 1986; Bronsky and associates,
submitted, 1989).
The principal parts affected are the position of nasal
placodes and improper fusion of the Medial Nasal Processes.
Cigarette smoking is found to double the incidence of CL/P.
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23. DRUG- INDUCED Aminopterin is the only drug that can produce Cleft Palate.
The incidence of CL/P in the children of epileptic mothers taking
anticonvulsant drugs like Phenytoin7
is approx. ten times to those
not taking the drug.
There is a reduction in the rate of cell multiplication in facial
region to approximately 50 per cent in such patients. (Hicks,
Johnston, and Banes, 1983).
The lateral nasal process is severely affected, leading to
interference with oxidative metabolism and improper placode
positioning.
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24. VITAMIN LEVELS DURING
PREGNANCY
There is evidence that deficiencies of key vitamins such as
folic acid, which are, involved in nucleotide (DNA and
RNA) synthesis and thus, important for cell proliferation, can
cause CL/P experimentally (Asling, 1961).3
Vitamin A, a fat-soluble vitamin is difficult to excrete out
and may be teratogenic at high levels (Cohlan, 1953).
A study conducted at the Centers for Disease Control
(CDC) indicates that ordinary vitamin supplements can
reduce the clefting incidence by more than 20 per cent
(Erickson, 1989).
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25. EMBRYOLOGY
The first pharyngeal arch (mandibular arch),
develops two prominences:
The maxillary prominence
The mandibular prominence
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29. As the medial nasal prominences merge with the maxillary
prominence, they form an intermaxillary segment.
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30. The intermaxillary segment gives rise to :-
1. philtrum of the upper lip.
2. The premaxillary part of the maxilla
3. The primary palate.
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32. Local Factors:
•Failure of the head to elevate and become erect at around the
7-9th
week
•Failure of the tongue to descend downwards, thus causing a
mechanical interference to fusion of the palatine shelves.
•Deficiency of Oxygen
•Shift of Blood Supply of Face-During the 6th
week, most of the
midface is supplied by the Stapedial artery which is the branch
of the Internal Carotid artery.
At around the 7th week, stapedial artery arises from the
internal carotid and its terminal branches join the external
carotid artery. Delay in this vital step can lead to cleft palate.
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34. DAVIS AND RITCHIE CLASSIFICATION
(1922):
They classified congenital clefts based on the position of the cleft in relation to
the alveolar process.
Group I-Pre alveolar clefts Lip
clefts only with subdivisions for
unilateral, median, bilateral.
Group II-Post alveolar clefts
degrees of involvement of soft and
hard palate to be specified till the
alveolar ridge, submucous clefts
included.
Group III-Alveolar clefts is
complete clefts of palate, alveolus
ridge and lip with subdivisions for
unilateral, median, bilateral.
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35. VEAU’S CLASSIFICATION
(1931):
Group I - Cleft of
soft palate only
Group IIGroup II - Cleft of hard and- Cleft of hard and
soft palate, extending nosoft palate, extending no
further than the incisivefurther than the incisive
foramen thus involving theforamen thus involving the
secondary palate alone.secondary palate alone.
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36. Group III - Complete
unilateral cleft of soft and
hard palate, lip and
alveolar ridge
Group IV - CompleteGroup IV - Complete
bilateral cleft of soft andbilateral cleft of soft and
hard palate, lip andhard palate, lip and
alveolar ridge on bothalveolar ridge on both
sides.sides.
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37. KERNAHAN’S STRIPED “Y”
CLASSIFICATION (1971):
In this classification the incisive
foramen is taken as the reference
point
“Y” logo are each divided into three
sections, representing the lip, the
alveolus and the hard palate as far
back as the incisive foramen. The
stem of the “Y” is also divided into
three parts, representing varying
degrees of clefting of the hard and
soft palates.
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38. MILLARD’S CLASSIFICATION (1977):
A modification of Kernahan’s
striped “Y” classification.
The inverted triangles
represent the nasal arch the
upright triangles represent
the nasal floor.
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39. FEEDING TECHNIQUES
When a cleft lip is present, it may be difficult forWhen a cleft lip is present, it may be difficult for
the baby to make a good seal around the nipple.the baby to make a good seal around the nipple.
Babies with cleft palate usually need special bottlesBabies with cleft palate usually need special bottles
and techniques to feed properly.and techniques to feed properly.
There are three types of bottles for feeding babiesThere are three types of bottles for feeding babies
with clefts –with clefts –
the Mead-Johnson Cleft Palate Nurser,the Mead-Johnson Cleft Palate Nurser,
the Haberman Feeder andthe Haberman Feeder and
the Pigeon Nipple:the Pigeon Nipple:
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40. Feeding obturatorFeeding obturator
The feeding obturator is a prosthetic aid that is designedThe feeding obturator is a prosthetic aid that is designed
to obturate the cleft and restore the separation betweento obturate the cleft and restore the separation between
the oral and nasal cavitiesthe oral and nasal cavities..
It creates a rigid platformIt creates a rigid platform
The obturator also prevents the tongue from entering theThe obturator also prevents the tongue from entering the
defectdefect and interfering with spontaneous growth of theand interfering with spontaneous growth of the
palatal shelves.palatal shelves.
Reduces nasal regurgitation,Reduces nasal regurgitation,
Reduces the incidence of chokingReduces the incidence of choking,,
Helps in the development of the jaws and contributes toHelps in the development of the jaws and contributes to
speechspeech
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41. Pre-surgical period
Pre-surgical orthodontics was used in Europe/USA for over
30 years but did not demonstrate any long term benefits in
relation to:
1. Facial growth
2. Appearance
3. Speech
4. occlusion
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42. Deciduous dentition
No treatment provided in Oslo at this stage :
1. Dental irregularities are usually minor
2. No long-term benefits
3. Does not ensure normal eruption of permanent teeth.
4. Certain need of future orthodontic treatment.
Evaluation of super-numerary teeth.
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43. Mixed dentition ( preparation for bone graft )
The first alveolar bone graft was placed in 1977 in Oslo based
on the results of cancellous bone grafts by Boyne/Sands.
Height of the inter-dental septum assessed on intraoral
radiographs.
Best results achieved when grafting done prior to the eruption
of the permanent canine.
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44. Many of the orthodontic problems encountered at this
stage are effects of early surgical repair.
Problems frequently encountered :
- Malposed permanent incisors
- Posterior crossbite
- A-P molar discrepancies.
- Serial extraction
- Detection of dental anamolies.
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45. Maxillary incisors :
Often erupt rotated, retroclined and possibly in
anterior crossbite.
Corrected for esthetic reasons and to facilitate oral
hygiene ( labial archwire – 3/4 months )
Less severe cases can be treated with a maxillary
Hawley plate or a finger spring.
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47. Buccal crossbite:
attributable to segmental displacement corrected simultaneously
using a palatal arch auxillary spring / Quad helix / Removable
screws.
Segmental repositioning :
- Done just prior to the bone grafting procedure
- Lingual appliance kept for 3 months post-operatively i.e. to enable
the bone graft to maintain the transverse dimension of the basal
bone.
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49. - In pt’s with BCLP, the mobile premaxilla is stabilized with a
heavy rectangular archwire to ensure immobility.
A-P molar discrepancies : (cooper)
- In Cl II cases : cervical pull headgear
- In Cl III cases : reverse pull headgear (Delaire face mask) + chin
cup therapy.
- Care to be taken in relation to severe ant-post hypoplasia.
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50. Early Permanent dentition :
2 to 3 years after bone grafting usually when the cleft side
canine has erupted spontaneously through the graft or has been
surgically exposed
Every effort is made to mesialize the posterior teeth and to
correct maxillary hypoplasia.
Maxillary hypoplasia is a common problem encountered in
almost 25% of the cleft population – Ross (87)
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51. Methods of correcting Maxillary
hypoplasia
Reverse pull headgear
Distraction osteogenesis
Orhthognathic surgery
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52. RPHG v/s Distraction
Factors to be considered
1. Age and compliance of the patient
2. Amount of correction
3. Biomechanics ( Force Vector )
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57. Fixed appliance Therapy
Recognition of orthodontic limitations in correction of
malocclusion.
“Therapeutic diagnosis”
Rigidity in the construction of the appliance is necessary
Fixed palatal expansion devices
- Hyrax
- Niti Palatal expander
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58. Additional necessary treatment mechanics :
- Cervical pull headgear for anchorage
- Intermaxillary elastics
- Additional lingual root torque to maxillary incisors.
- Banding preferred to bonding.
- Orthodontic correction of lower arch delayed.
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59. Maximum treatment time not to exceed 2 yrs and to be
completed by the age of 18-20 yrs.
Bonded palatal retainer to extend to two teeth on either
side of the cleft.
Assess need for full-time retention.
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60. INFANT ORTHOPEDICS
Infant orthopedics was pioneered by Burstone at Liverpool in 1950s.
Two movements were carried out- expansion of the collapsed
segments and pressure against premaxilla to reposition it posteriorly
to its correct position.
Done by placing light elastic strap across the anterior segment that
applies a contraction force. In severe cases pin retained appliances
may be required.
Also consists of a feeder plate with steel
wires bent in to hooks incorporated into the
acrylic.
After active treatment for 3-6weeks,it is
used a retainer.
Berkowitz reported the present consensus is
that these procedures offer less long term
benefit than expected. Hence now used in
severely displaced premaxilla cases.
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61. • Displacement of segment make lip
repair more difficult
• Orthopaedic appliances are used to
resposition the segment in early infancy,
before lip closure
• These appliances also act as “feeding
plate” for infants
• Two types of orthopaedic appliancesTwo types of orthopaedic appliances
ActiveActive
PassivePassive
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62. Naso Alveolar Moulding
Nasoalveolar molding is a nonsurgical method of reshaping the
gums, lip and nostrils before cleft lip and palate surgery,
reducing the severity of the cleft. Surgery is performed after the
molding is complete, approximately three to six months after
birth.
PRESURGICAL NASO ALVEOLAR MOLDING
(Grayson etal, 1999)
Actively mold and reposition the deformed nasal cartilages and
alveolar processes and lengthen the deficient collumella.
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64. Procedure
Impressions of the infant are made using an
elastomeric impression material
Impressions of the cleft are useful in
assessing pre and post alveolar molding
results and also in fabrication of the nasal
stent.
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65. Fabrication of molding
plate
A molding plate is fabricated using
conventional acrylic resin
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66. The molding plate is secured to the palate
and alveolar process through external
strapping (surgical adhesive tapes) to the
cheeks and to an acrylic extension from the
oral plate between the lips below the cleft.
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69. LIP CLOSURELIP CLOSURE
Surgical closure of a cleft lip is done as early inSurgical closure of a cleft lip is done as early in
infancy (at 10 to 12 weeks of age) as isinfancy (at 10 to 12 weeks of age) as is
compatible with a good long-term result.compatible with a good long-term result.
Therefore PNAM should be completed byTherefore PNAM should be completed by
then.then.
TechniquesTechniques
Rotation-advancement technique of MillardRotation-advancement technique of Millard
Delaire philosophyDelaire philosophy
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70. PALATE CLOSUREPALATE CLOSURE
Objective:Objective:
• Join the cleft palatal edges,Join the cleft palatal edges,
• Lengthen the soft palate,Lengthen the soft palate,
The timing of closure is controversial. Can beThe timing of closure is controversial. Can be
done early at 18-24 months or at 9-12yeardone early at 18-24 months or at 9-12year
At 18-24 month-At 18-24 month-
Development of normal speechDevelopment of normal speech
Tendency towards maxillary underdevelopmentTendency towards maxillary underdevelopment
At 9-12year-At 9-12year-
Normal growth of maxilla with unrepaired cleftNormal growth of maxilla with unrepaired cleft
Reduces surgical morbidity and infectionReduces surgical morbidity and infection
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71. Latest suggestion-Latest suggestion-
Closure of soft palate –age of 12 monthClosure of soft palate –age of 12 month
Help in development of SpeechHelp in development of Speech
No growth retardation with early soft palateNo growth retardation with early soft palate
closureclosure
Closure of hard palate –age of 5-6yearClosure of hard palate –age of 5-6year
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72. Velopharyngeal Insufficiency
Velopharyngeal insufficiency is a disorder resulting in the
improper closing of the velopharyngeal sphincter (soft
palate muscle in the mouth) during speech, allowing air to
escape through the nose instead of the mouth.
During speech, the velopharyngeal sphincter must closeDuring speech, the velopharyngeal sphincter must close
off the nose to properly pronounce strong consonantsoff the nose to properly pronounce strong consonants
such as "p," "b," "g," "t" and "d."such as "p," "b," "g," "t" and "d."
The two main speech symptoms of velopharyngealThe two main speech symptoms of velopharyngeal
insufficiency are:insufficiency are:
hypernasality andhypernasality and
nasal air emission.nasal air emission.
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73. Treatment of VPI
Speech Therapy
Some speech problems linked with VPI, such as
mispronouncing words, can be treated by speech therapy.
Treatment focuses on teaching the child the correct
manner and place of articulation
Sometimes an obturator is recommended to treat VPI.Sometimes an obturator is recommended to treat VPI.
An obturator is like a modified dental retainer with aAn obturator is like a modified dental retainer with a
speech bulb or palatal lift attached to the back. Eachspeech bulb or palatal lift attached to the back. Each
obturator is shaped uniquely to fit the patient’s muscleobturator is shaped uniquely to fit the patient’s muscle
movements.movements.
Speech Surgery: PalatoplastySpeech Surgery: Palatoplasty
Sphincter pharyngeoplastySphincter pharyngeoplasty
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75. Cleft lip and palate cont…
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76. Lahshal classification: (1987)
This is simple classification presented by Okriens in 1987.
L A H S H A L is paraphase of the anatomic areas affected
by the cleft.
L-Lip A-Alveolus H-Hard palate S-Soft palate H-Hard
palate A-Alveolus L-Lip
This classification is based on the fact that clefts of lip,
alveolus, hard palate can be bilateral while clefts involving
the soft palate are usually unilateral.
Areas involved in the cleft are denoted by specifically
indicating the alphabet for it.
For example
L_ _ S_ _ _ stands for cleft of right lip and soft palate.
LA_S_ _L stands for cleft of the right lip, alveolus, and soft
palate together with left cleft lip.
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79. Rationale for bone graftingRationale for bone grafting
To restore physiologic continuity of arch for esthetic andTo restore physiologic continuity of arch for esthetic and
hygenic replacementhygenic replacement
To provide bone for stability of dental arch and theTo provide bone for stability of dental arch and the
premaxillary segmentpremaxillary segment
Bone is provided into which unerupted teeth may erupt.Bone is provided into which unerupted teeth may erupt.
At the time of placement of graft, patent oronasal fistulasAt the time of placement of graft, patent oronasal fistulas
can be closed.can be closed.
To allow orthodontic alignment of teeth.To allow orthodontic alignment of teeth.
To provide support for the lip and the alar base and theTo provide support for the lip and the alar base and the
nasal tip.nasal tip.
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80. Primary Bone Grafting
Primary bone grafting in infants, was introduced in the
1950s.
Aims of Primary Bone Grafting
In this early surgical intervention, the cleft alveolus and palate
were united by filling the cleft defect with autogenous bone,
typically a spilt-rib graft.
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81. Timing of Bone Graft
Primary bone grafting coincides with surgical repair of
the lip and therefore occurs during infancy, although its effect
is not appreciated fully until growth and development of the
maxilla are complete.
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82. Results of Primary Bone Graft
Early results in the 1950s gained popularity because of
the advantages associated with this technique, including
prevention of maxillary arch collapse and normal development
of the craniofacial complex. Migration of teeth into the grafted
area was observed. Comparisons between patients who had
undergone primary bone grafting and those who had not
indicated that early bone grafting compromised growth of the
midface and resulted in a higher incidence of malocclusion
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83. Secondary Bone Grafting
Secondary or delayed alveolar bone grafting is
performed after primary lip repair.
The introduction of secondary bone grafting of the
cleft maxilla and palate, was pioneered in Europe, was reported
in the German literature at the beginning of this century.
However, it was not until the 1970’s that secondary or delayed
bone grafting became popular in the United States.
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84. Timing of Secondary Bone Graft
Early Secondary Bone Grafting (2-5
years of Age)
This typically is performed during the primary dentition
period (age range, 2-5 years). According to advocates of this
relatively early timing of grafting, the bony support for the
future eruption of the lateral permanent incisor is an important
consideration in the periodontal health of this tooth adjacent to
the cleft site.
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85. Intermediate or Secondary Bone
Grafting (6-15 Years of Age)
Contemporary opinion is that this is the optimal time for
alveolar bone grafting. Bone is provided for the eruption of the
permanent canine into the cleft site; this has the added advantage
of including alveolar bone with the eruptive process. Minimal
interference in midfacial growth and development can be
expected.
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86. Late Secondary Bone Grafting
(Adolescence to Adulthood)
Reconstruction in the skeletally mature patient with a
cleft does not involve the same requirements as in younger
patients. The need for a graft material to allow eruption of teeth
through the graft into the dental arch is obviated, and
replacement of missing teeth by implants is a consideration,
especially in the non growing patient.
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87. Type of Grafting Material
Autogenous bone grafts
Allogeneic bone grafts
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88. Documented clinical studies indicates that autogenous
cancellous bone is the preferred and most successful grafting
material. From the surgeon’s perspective the most popular
donor site has been iliac crest, although the morbidity associated
with harvesting cancellous bone from the hip has resulted in
alternative sites.
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89. Early versus Delayed PalateEarly versus Delayed Palate
RepairRepair
Speech
Dentofacial
Growth
Ideal age for palate repair still disputed
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90. PALATE CLOSUREPALATE CLOSURE
The timing of closure is controversial. Can beThe timing of closure is controversial. Can be
done early at 18-24 months or at 9-12yeardone early at 18-24 months or at 9-12year
At 18-24 month-At 18-24 month-
Development of normal speechDevelopment of normal speech
Tendency towards maxillary underdevelopmentTendency towards maxillary underdevelopment
At 9-12year-At 9-12year-
Normal growth of maxilla with unrepaired cleftNormal growth of maxilla with unrepaired cleft
Reduces surgical morbidity and infectionReduces surgical morbidity and infection
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92. Philadelphia Centre for research in Child
growth-Wilton Krogman(1947-71)
Divided into EIGHT STAGES
First stage-Prenatal phase-
Complete history of gestation and maternal health taken.
This is accompanied by counseling of the parents. All this is
carried out by the Genetisist and other Social workers.
Second stage – at birth
At this stage pediatrician discusses the condition with the
parents.Surgeon advises about the operative plan and the
dental specialists appraises the arch relationships.
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93. Third stage – birth to 1 year
Pediatrican –advises about the feeding etc.
Surgeon- carries out the lip closure (rule of 10)
Dental specialist-secures the models and radiographs etc.
Speech therapist- discusses about the insufficiency and
incompetence of the pharyngeal seal.
Fourth stage -1-2yrs
Pediatrican-takes care of the health and nutrition.
Speech therapist-monitors the vocabulary and option of a
prosthetic replacement
ENT-monitors the ear condition
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94. Fifth stage-2-6yrs
Role of Orthodontist –arch relations
- Crossbites
- Developing malocclusion.
Sixth stage -6-12yrs
Surgical corrections-secondary closure /repair of palate, lip and
the nose.
Seventh stage-12-18 yrs
Surgical follow up on the lip and nose corrections orthodontic
treatment is continued
Eighth stages- 18 yrs onwards.
Regular follow up of the patient ,this can be done by a general
practitioner
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95. Cleft Lip and Palate Patients Management in
OSLO-Norway
Lise and Ramstand 1948
•No preoperative orthopedics.
•Closure of Cleft lip in infancy using millard procedure -3
months
The primary closure of lip and nasal floor in a combined cleft
lip and palate leaves the posterior defect like an isolated palate
and then repair later.Closure of the alveolar cleft region by a
one layer flap during primary lip repair.
•Closure of the remaining isolated cleft –Von Langenbeck -18
months.
•Secondary operations 18-30 yrs of age.
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96. Latest suggestion – B . NandlalLatest suggestion – B . Nandlal
Closure of soft palate –age of 12 monthClosure of soft palate –age of 12 month
Help in development of SpeechHelp in development of Speech
No growth retardation with early soft palateNo growth retardation with early soft palate
closureclosure
Closure of hard palate –age of 5-6yearClosure of hard palate –age of 5-6year
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97. Chronology of Team Cleft CareChronology of Team Cleft Care
ProceduresProcedures (Smile train).(Smile train).
At birth………..Reassurance, counseling and feedingAt birth………..Reassurance, counseling and feeding
instructionsinstructions
3 months……..Lip surgery3 months……..Lip surgery
6 months……..Pediatric dental care6 months……..Pediatric dental care
12-18 months. Palate repair followed by Pediatric dental12-18 months. Palate repair followed by Pediatric dental
care and blowing exercisescare and blowing exercises
36 months……Speech and ENT consultation36 months……Speech and ENT consultation
48-60 months. Orthodontic review / intervention48-60 months. Orthodontic review / intervention
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98. Chronology of Team Cleft CareChronology of Team Cleft Care
Procedures (contd.)Procedures (contd.)
5-6 years……Columellar lengthening and sulcus repair5-6 years……Columellar lengthening and sulcus repair
4-10 years….Definitive speech therapy4-10 years….Definitive speech therapy
5-10 years….Maxillary growth modulation5-10 years….Maxillary growth modulation
7-10 years….Incisor correction7-10 years….Incisor correction
9-12 years….Arch preparation for alveolar bone graft9-12 years….Arch preparation for alveolar bone graft
11-20 years…Comprehensive orthodontics11-20 years…Comprehensive orthodontics
16-21 years…Orthognathic surgery and rhinoplasty16-21 years…Orthognathic surgery and rhinoplasty
16-21 years…Final touch ups for lip and nose after16-21 years…Final touch ups for lip and nose after
active orthodonticsactive orthodontics
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99. 0 3 6 9 12 15 18 21 24
Chronology and Duration of Team Cleft Care Events
(birth to 24 months)
Pediatric Dental Care
Lip
Repair
Reassurance,
Counselling,
Feeding
Instructions…
Palate Repair
Blowing exercises
Age in Months
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100. 3 6 9 12 15 18
21
Chronology and Duration of Team Cleft Care Events
( 3 years to adulthood )
Age in Years
Speech &
ENT
Consultation
Speech Therapy
Sulcus
repair &
columellar
lengthening
Max. Growth
Modul. Arch Prep. &
Alv. Bone
graft
Pediatric Dental Care
Comprehensive orthodontics
Orthognathic
Surgery
Final touch ups
General Dental Care
Prosthetic
rehab.
Secondary Surgical Procedures
Palate redo, Pharyngoplasty, Tongue flap, Rhinoplasty etc.
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101. Timing of Primary CleftTiming of Primary Cleft
SurgeriesSurgeries
Lip repair………….3 months (Rule of 10)Lip repair………….3 months (Rule of 10)
above 10 wks. Ageabove 10 wks. Age
above 10 Gm. Hb.above 10 Gm. Hb.
above 10 Lbs. Wt.above 10 Lbs. Wt.
Palate repair……....12-18 monthsPalate repair……....12-18 months
No anesthetic risk and manageable tissuesNo anesthetic risk and manageable tissues
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102. In Utero Cleft Palate Repair -
John Canady 1993
Five ewes were operated on ranging in gestation from 70
to 133 days.
Animals operated at 112 days or later in gestation
exhibited scars both clinically and histologically.
The animals that had cleft palate produced and repaired at
70 days gestation did not have a visible palatal scar at 1
month of age.
Histologically, there was evidence of minimal scarring
without disruption of normal architecture.
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103. Adverse Outcomes Following Endoscopic Repair of
a Fetal Cleft Lip
None of the five fetuses reported here had a good aesthetic
result.
Although there was no evidence of scar histologically, the
edges of the lip were poorly approximated.
The epithelial lining and underlying dermis of the wound
margins were notably inverted.
The orbicularis oris muscle, which had been reapproximated,
appeared thin and hypoplastic.
Most of the vermilion elements were poorly aligned, and in
one animal, there was a complete dehiscence of the repair.
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104. The fetal cleft palate: IV. Midfacial growth and bony palatal
development following in utero and neonatal repair of the
congenital caprine model - Weinzweig J et al 2006
1. In utero cleft palate repair does not contribute to impairment of midfacial
growth.
2. The authors attribute this finding to the scarless nature of mucoperiosteal
healing in the privileged fetal environment.
3. Cleft repair in the newborn period, or thereafter, results in midfacial growth
impairment due to the scarring that routinely accompanies conventional
palatoplasty.
4. The combination of the growth impairment inherent in the cleft anomaly and
that attributable to postnatal repair scarring yields the midfacial retrusion
commonly associated with cleft palate.
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105. DISTRACTION OSTEOGENESISDISTRACTION OSTEOGENESIS
1903 . Dr. Gavril of Russia-Bone lengthening of leg.1903 . Dr. Gavril of Russia-Bone lengthening of leg.
It is a procedure that moves two segment of boneIt is a procedure that moves two segment of bone
slowly apart in such a way that new bone fills theslowly apart in such a way that new bone fills the
gap.gap.
In distraction osteogenesis, a surgeon makes anIn distraction osteogenesis, a surgeon makes an
osteotomy in an bone and attaches a deviceosteotomy in an bone and attaches a device
known as distractor to both sides of osteotomy.known as distractor to both sides of osteotomy.
The distractor is gradually adjust over a period ofThe distractor is gradually adjust over a period of
days or week to stretch the osteotomy so newdays or week to stretch the osteotomy so new
tissue fills it.tissue fills it.
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106. Ross and Subtenly said that, Distraction osteogenesis allows soft
tissue adaptation, including scar tissue. Therefore doesn’t cause a
problem with vello- pharyngeal insufficiency thus gives good results.
Distraction Of maxilla first proposed by Molina & Oritz-
Monasterio(1998)
EXTERNAL DISTRACTORS
Advantage:
•Direction of force is well
controlled
Dis advantage:
•Cranial surgery is required
•Esthetics are compromised
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108. CONCLUSION
Clefts have been identified to have a multifactorialClefts have been identified to have a multifactorial
etiology and therefore require an interdisciplinaryetiology and therefore require an interdisciplinary
treatment approach, comprising a team effort intreatment approach, comprising a team effort in
which an orthodontist plays a vital role and workswhich an orthodontist plays a vital role and works
hand in hand with various specialists to provide thehand in hand with various specialists to provide the
best possible line of treatment with a single mindedbest possible line of treatment with a single minded
approach , that is to minimize if not eliminate theapproach , that is to minimize if not eliminate the
physical, social and the emotional hardship that aphysical, social and the emotional hardship that a
person with orofacial cleft presents.person with orofacial cleft presents.
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109. REFRENCES
1. Berkowitz S.- The Cleft Palate Story, 1994,
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2. Sadove A.Michael,Van Aalst John, Culp John
Andrew- Cleft Palate Repair: Art And Issues;
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Craniofacial Anomalies, Ed 3, Philadelphia,
1990, Saunders.
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6. Peterson, Ellis, Hupp, Tucker; Contemporary Oral And
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12. Baik. Surgical Orthodontic Treatment In Patients
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13. Robert .M. Manson -Clinical Aid –A Retraction For
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16. Michel .O.Abdoney -Use Of The Arndtnickel Tit
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18. H.S.Orton. J.H.Noar, -The Customized Facemask –
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22. Slavkin And Melnick-Maternal Influcences Of Congenitial
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34. Weinzweig J, Panter KE, Seki J, Pantaloni M,
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